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Hypovolemic shock in children: Initial evaluation and management

Hypovolemic shock in children: Initial evaluation and management
Literature review current through: Sep 2023.
This topic last updated: Jan 28, 2022.

INTRODUCTION — This topic will review the evaluation and treatment of hypovolemic shock in children. A general approach to the initial evaluation and management of shock in children, evaluation and treatment of hypovolemia in children, and the pathophysiology of shock are discussed separately:

(See "Initial evaluation of shock in children".)

(See "Initial management of shock in children".)

(See "Clinical assessment of hypovolemia (dehydration) in children".)

(See "Treatment of hypovolemia (dehydration) in children in resource-abundant settings".)

(See "Pathophysiology and classification of shock in children".)

TERMINOLOGY — Hypovolemic shock is characterized by inadequate tissue perfusion from decreased intravascular volume as the result of fluid loss and/or inadequate fluid intake.

ETIOLOGY — Sources of volume loss that can lead to hypovolemic shock include the following [1]:

Diarrhea and/or vomiting

Hemorrhage

Osmotic diuresis (eg, hyperglycemia)

Capillary leak (eg, sepsis, intraabdominal processes with third space losses [eg, pancreatitis, intussusception, appendicitis], or burn injury)

Inadequate fluid intake (particularly among infants and young children who cannot independently access fluids to replenish losses)

Insensible losses (eg, fever or burns)

Worldwide, hypovolemic shock from diarrheal disease is a major cause of death among all children younger than five years of age and is especially prevalent in those living in resource poor countries [2].

Hemorrhagic shock in children is most often the result of major trauma. Less common causes include gastrointestinal bleeding, postoperative bleeding, and pulmonary hemorrhage. Sickle cell anemia complicated by sequestration crisis can result in physiologic complications similar to hemorrhagic shock. (See "Pediatric blunt abdominal trauma: Initial evaluation and stabilization" and "Overview of the clinical manifestations of sickle cell disease".)

PATHOPHYSIOLOGY AND CLASSIFICATION — Hypovolemic shock develops when intravascular volume is insufficient to maintain tissue perfusion. Fluid losses may be strictly intravascular (eg, hemorrhage, third-space losses from intraabdominal processes [eg, pancreatitis, intussusception, appendicitis] or capillary leak), a combination of intravascular and extravascular (eg, burn injury), or primarily extravascular (eg, diarrheal disease). (See "Clinical assessment of hypovolemia (dehydration) in children", section on 'Type of fluid lost'.)

Initial compensation for volume depletion includes stimulation of thirst and fluid conservation by the kidneys. The following mechanisms come into play once perfusion becomes compromised [1,3]:

Tachycardia increases cardiac output. However shortened ventricular filling time can result in decreased stroke volume and worsening cardiac output.

Increased systemic vascular resistance (SVR), mediated by the sympathetic nervous and renin-angiotensin systems, results in redistribution of blood flow from peripheral structures (including skin, muscle, kidneys, and splanchnic organs) to the heart and central nervous system.

Increased cardiac contractility can maintain stroke volume by increasing ventricular emptying.

Among children with hypovolemic shock, hypotension develops late, and may signal impending cardiac arrest [3]. Compensatory vasoconstriction maintains blood pressure at the expense of reduced tissue perfusion. As a result, hypovolemic shock progresses rapidly to cardiovascular collapse and cardiac arrest once hypotension develops. (See "Pathophysiology and classification of shock in children".)

Hypovolemia can be classified by the degree of volume depletion, with patients in shock included in the most severe categories.

For children with nonhemorrhagic losses, volume depletion is characterized as mild, moderate, or severe depending upon the percent loss of body weight: 3 to 5 percent (mild), 6 to 9 percent (moderate), and 10 percent or more (severe). Clinical features are typically used to estimate volume deficit since premorbid weight is usually not known (table 1). Many children with moderate volume depletion and all of those with severe depletion have compromised perfusion and are in shock. (See "Clinical assessment of hypovolemia (dehydration) in children", section on 'Estimating degree of hypovolemia'.)

Patients with hemorrhage can be categorized by severity into four classes based upon percent loss of blood volume. As with nonhemorrhagic losses, clinical features are typically used to estimate blood volume deficit (table 2). Many children with class II hemorrhage and all of those with classes III and IV are in shock. The approach to hemorrhage by class is as follows:

Class I – Class I hemorrhage occurs with acute loss of up to 15 percent of the child's blood volume. Minimal physiologic changes are evident and patients usually respond well to crystalloid fluid replacement.

Class II – Class II hemorrhage results from 15 to 30 percent blood loss. Physiologic changes include mild tachycardia and tachypnea with a narrow pulse pressure, slightly delayed capillary refill, decreased urine output, and mild anxiety. Patients can usually be stabilized with crystalloid solution, although they may require blood products.

Class III – Class III hemorrhage is the result of an acute blood loss of 30 to 40 percent. Signs of shock (including tachycardia, tachypnea, hypotension, delayed capillary refill, altered mental status, and oliguria) are present. Prompt resuscitation with crystalloid solution is necessary; most patients will need blood products as well.

Class IV – Class IV hemorrhage occurs with more than 40 percent acute blood loss. Signs of shock are obvious and immediately life-threatening. Patients are usually cold and pale with profoundly depressed mentation, marked tachypnea and tachycardia, and anuria. Children should quickly receive blood products. Operative intervention is often necessary to control hemorrhage.

EVALUATION — Clinical characteristics associated with imminent cardiovascular collapse must be quickly identified with an initial rapid assessment. Children who have been injured and have hemorrhagic hypovolemic shock may have associated injuries that require stabilization (ie, cervical spine immobilization for suspected neck injury or needle thoracostomy for tension pneumothorax). An approach to rapidly identifying the cause of shock based upon clinical findings is provided in the algorithm (algorithm 1). (See "Initial evaluation of shock in children", section on 'Rapid assessment'.)

History — Historical features typically suggest the source of volume loss (ie, vomiting and diarrhea with gastroenteritis, osmotic diuresis with diabetic ketoacidosis, insensible and capillary leak following burn injury, third space losses with intraabdominal processes [eg, pancreatitis, intussusception, small bowel obstruction], sickle cell disease with splenic sequestration crisis, or hemorrhage with blunt abdominal trauma).

Additional key historical information to consider includes:

The type of fluid loss may influence fluid management (ie, blood transfusion for children with hemorrhage or isotonic fluids followed by slower administration of hypotonic fluids in patients with hypernatremic dehydration). (See "Treatment of hypovolemia (dehydration) in children in resource-abundant settings", section on 'Hypernatremia'.)

Prior fluid replacement may cause abnormalities in serum electrolyte levels (ie, hyponatremia from fluid replacement with free water, typically in young infants). (See "Treatment of hypovolemia (dehydration) in children in resource-abundant settings", section on 'Hyponatremia'.)

Physical examination — Physical findings for children with hypovolemic shock are similar to those of patients with shock from other causes. (See "Initial evaluation of shock in children", section on 'Physical examination'.)

These include:

Signs of decreased cerebral perfusion (ie, poor tone, unfocused gaze, listlessness, or decreased responsiveness to caretakers or painful interventions)

Signs of poor peripheral perfusion (ie, decreased or absent distal pulses, cool extremities, prolonged capillary refill [>2 seconds])

Specific features of the physical examination that may be noted in children with hypovolemic shock include:

Children who are hypotensive with histories of trauma are likely in hemorrhagic shock. They must be carefully evaluated to identify sources of bleeding and associated injuries (table 3). (See "Trauma management: Approach to the unstable child".)

Children with hypovolemic shock typically have narrow pulse pressures as the result of elevated diastolic pressure from increased systemic vascular resistance.

Signs of significant volume loss may be less dramatic among children with hypertonic dehydration (as can occur with hypotonic fluid loss from conditions such as rotavirus gastroenteritis and arginine vasopressin deficiency or resistance [previously called central or nephrogenic diabetes insipidus, respectively]). This is because the associated increase in serum osmolality pulls water out of the cells, initially minimizing the degree of extracellular fluid volume loss. (See "Clinical assessment of hypovolemia (dehydration) in children", section on 'Type of fluid lost'.)

Abdominal distention, mass, or tenderness is consistent with an abdominal catastrophe, such as bowel obstruction, perforation, or peritonitis. Inflicted injury should be suspected in the absence of a history of trauma. (See "Physical child abuse: Recognition", section on 'Red flag history' and "Physical child abuse: Recognition", section on 'Visceral injuries'.)

Ongoing losses must be identified (ie, persistent vomiting, diarrhea, or active bleeding). They may need to be replaced and/or treated.

Children with moderate to severe burns are at increased risk of hypovolemia due to insensible losses. (See "Moderate and severe thermal burns in children: Emergency management", section on 'Evaluation of burn injury'.)

Ancillary data — The diagnosis of hypovolemic shock usually is based upon physical signs and symptoms. Once fluid therapy is initiated, ancillary data can be useful to detect associated electrolyte and acid-base abnormalities and to guide treatment.

Laboratory evaluation

Hypovolemic shock without hemorrhage – The following studies are suggested in children with hypovolemic shock without hemorrhage:

Rapid blood glucose – Children with hypovolemic shock from gastroenteritis are at risk for hypoglycemia. In contrast, pediatric trauma and burn victims commonly have hyperglycemia caused by physiologic stress. In some of these patients, the blood glucose can exceed 300 mg/dL (16.7 mmol/L) with the potential to cause an osmotic diuresis [4].

Electrolyte levels – Abnormalities in serum sodium and potassium levels may occur among children with hypovolemic shock. Serum sodium concentrations are influenced by the type of fluid loss, secretion of antidiuretic hormone, and prior fluid replacement. Clinical features that affect serum potassium include type of fluid loss (ie, increased loss in diarrheal stool) and the degree of acidosis (with marked acidosis, serum potassium concentration may be increased). Serum and urine electrolyte testing in hypovolemia is discussed separately. (See "Clinical assessment of hypovolemia (dehydration) in children", section on 'Laboratory testing'.)

Creatinine – A baseline measurement of serum creatinine and early monitoring of urine output are essential to promptly identify acute kidney injury, which may develop in children with hypovolemic shock. (See "Acute kidney injury in children: Clinical features, etiology, evaluation, and diagnosis".)

Lactic acid – Although evidence is lacking, lactic acid measurement may be helpful in the initial evaluation of hypovolemic shock. Based on observational studies in children with septic shock, hypoperfusion should be suspected when the lactate is >2 mmol/L (18 mg/dL). Initial lactate levels >4.0 mmol/L (36 mg/dL) are associated with increased mortality in children. (See "Systemic inflammatory response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Laboratory studies'.)

Lactic acid measurement may be helpful in the initial evaluation of shock. Lactate levels >5 mmol/L are associated with increased mortality in children [5,6]. When shock is masked by “normal” blood pressure for age, a blood lactic acid level >4 mmol/L usually indicates shock, even without overt clinical signs of hypoperfusion. Hypoperfusion may be masked by normal blood pressure. Although evidence is limited in children, studies in adults show that initial lactate levels are better than blood pressure at predicting mortality. (See "Evaluation and management of suspected sepsis and septic shock in adults".)

Urine dipstick – Rapid urine dipstick provides a quick measurement of the urine specific gravity, ketones, and glucose. Glycosuria with ketones suggests diabetic ketoacidosis.

Other – Other laboratory studies (eg, liver enzymes [alanine aminotransferase (ALT) and aspartate aminotransferase (AST)], albumin, protein, and coagulation studies in patients with hypovolemic shock and suspected liver dysfunction) may be indicated based upon the suspected etiology.

Hemorrhagic hypovolemic shock – In addition to the studies suggested above, children with hemorrhagic hypovolemic shock warrant the following studies:

Hematocrit – Most children with hemorrhagic shock have acute blood loss. The initial hematocrit is typically normal because equilibration with extracellular fluid has not yet occurred. However, the hematocrit will drop with repeated measurements over time. Patients with hemorrhagic shock and a low initial hematocrit often have life-threatening hemorrhage.

In patients with hypovolemic shock primarily from fluid losses such as diarrhea, the hematocrit may be elevated due to hemoconcentration.

Coagulation studies (platelet count, PT, aPTT and INR, fibrinogen) – Coagulation studies are indicated in patients with ongoing hemorrhage and any of the following conditions:

-Known or suspected thrombocytopenia (eg, post-chemotherapy, bone marrow transplant, ITP, etc)

-Liver dysfunction

-Anticoagulant therapy

-Severe penetrating or blast trauma [7]

-Massive transfusion (volume of blood received equivalent to total blood volume), or with significant bleeding to the extent that their clotting ability has been diminished

The hemorrhage may not stop until coagulation parameters are corrected. Thus, evaluation of platelet count, PT, and PTT can assist in identifying coagulopathy and guiding correction with platelet infusion and/or fresh frozen plasma. Liver enzymes (ALT and AST), albumin, protein, and fibrinogen should also be checked in patients with liver dysfunction because cryoprecipitate may be needed to more effectively replace liver-dependent clotting factors (factors II, VII, IX, and X).

Type and cross match – Children with hemorrhagic shock may require urgent transfusion. Although typed and cross-matched blood products are preferred, they may take 30 to 45 minutes to prepare. Type-specific blood can usually be obtained within 15 to 20 minutes. Type O, Rh-negative blood for females and type O, Rh-negative or Rh-positive blood for males can be used for patients who require immediate transfusion. Hypocalcemia and coagulation abnormalities may develop in patients who require massive transfusion. Better outcomes may be achieved by ensuring coadministration of platelets and fresh frozen plasma as part of a massive transfusion protocol. The ratio of blood products and the indications for initiating such a protocol in children is discussed separately. (See "Trauma management: Approach to the unstable child", section on 'Blood products' and "Massive blood transfusion".)

Blood gas measurements – Patients with hypovolemic shock develop lactic acidosis caused by inadequate tissue oxygenation and perfusion. Thus, metabolic acidosis is typically present on arterial or venous blood gases. Metabolic acidosis can also be evident by lowered carbon dioxide measurements obtained by capnography. (See "Carbon dioxide monitoring (capnography)", section on 'Detecting metabolic acidosis'.)

Other studies — A chest radiograph can be useful to evaluate heart size for children with apparent hypovolemic shock who do not improve following the administration of 60 mL/kg of fluid. If the heart size is small, then additional bolus fluid administration is indicated. In contrast, if the heart is big, then fluid therapy should be moderated and additional types of shock (eg, septic or cardiogenic shock) may be present and warrant specific therapy. (See "Septic shock in children: Rapid recognition and initial resuscitation (first hour)" and "Initial management of shock in children", section on 'Further management by type of shock'.)

For patients with traumatic hemorrhagic shock, a chest radiograph may identify intrathoracic bleeding or other causes for shock, such as tension pneumothorax or pericardial effusion. (See "Trauma management: Approach to the unstable child", section on 'Screening radiographs'.)

For children with trauma, additional imaging (eg, focused assessment with sonography in trauma [FAST] or computed tomography) is typically warranted. The approach to imaging in the pediatric trauma patient is discussed separately. (See "Trauma management: Approach to the unstable child", section on 'Adjuncts to the primary survey' and "Trauma management: Approach to the unstable child", section on 'Adjuncts to the secondary survey'.)

Although evidence is limited, point-of-care ultrasound is an emerging diagnostic modality for rapidly evaluating cardiac function and volume status in critically ill children, identifying the etiology of shock, and helping direct management. However, it requires training for proper application and interpretation [8,9].

MANAGEMENT — Successful management of children with hypovolemic shock requires identification and treatment of life-threatening conditions and the rapid initiation of aggressive fluid resuscitation. (See "Initial evaluation of shock in children", section on 'Rapid assessment'.)

Airway and breathing — For hemorrhagic hypovolemic shock due to blunt trauma, patients should have a rigid cervical collar in place and full spinal immobilization until a spinal fracture can be ruled out. (See "Trauma management: Approach to the unstable child", section on 'Airway with cervical spine motion restriction' and "Pediatric cervical spinal motion restriction" and "Evaluation and acute management of cervical spine injuries in children and adolescents".)

Airway management should include supplemental oxygen with an initial inspired concentration of 100 percent. Early positive pressure ventilation and intubation should be performed in patients with airway compromise or impending respiratory failure. A rapid overview provides the suggested approach to rapid sequence intubation in children (table 4). Children with hemodynamic instability from hypovolemic shock should receive sedation using either etomidate or ketamine prior to intubation. The clinician should avoid the routine use of etomidate in children who also have presumed (suspicion for) septic shock. (See "Technique of emergency endotracheal intubation in children" and "Rapid sequence intubation (RSI) in children for emergency medicine: Approach" and "Septic shock in children: Rapid recognition and initial resuscitation (first hour)", section on 'Airway and breathing'.)

Control of hemorrhage — Sites of significant external hemorrhage require direct manual pressure to control bleeding (figure 1). The presence of nerves near vascular bundles prohibits blind clamping of bleeding vessels except in the scalp. In patients whose bleeding does not abate with direct pressure or who have a sharp foreign body at the site of bleeding or an amputation, compression at the nearest vascular pressure point provides an alternative means for hemorrhage control (figure 2). In the combat theater, hemostatic gauze has been shown to be an effective adjunct for hemorrhage control in the prehospital setting and, if available, may be a helpful in the civilian setting when direct pressure is ineffective, especially for penetrating or junctional wounds (eg, high femoral vessel wound) not amenable to direct pressure or tourniquets [10,11]. Finally, the medical provider may employ a blood pressure tourniquet or Penrose drain tourniquet for severe bleeding that is poorly controlled despite direct pressure or compression of pressure points. (See "Trauma management: Approach to the unstable child", section on 'Hemorrhage control'.)

Severe bleeding from a large scalp laceration often responds to rapid closure using a figure of eight suture, surgical staples, or scalp clips (Raney clips). A circumferential Penrose drain tourniquet can provide temporary control of scalp bleeding until repair is complete (figure 3). (See "Closure of minor skin wounds with staples".)

Reduction and splinting of long bone fractures may also provide hemostasis. (See "Basic techniques for splinting of musculoskeletal injuries".)

For patients with a suspected pelvic fracture and hemodynamic instability, clinicians should carefully examine the perineum and rectum and then place a pelvic stabilization device over the greater trochanter (prefabricated pelvic binder or a bed sheet tied tightly around the pelvis) (figure 4). External fixation devices are generally placed in the operating room because placement can be difficult and time consuming and may interfere with other components of resuscitation. (See "Trauma management: Approach to the unstable child", section on 'Hemorrhage control'.)

For patients with pulmonary hemorrhage from a diffuse lung process, endotracheal intubation and mechanical ventilation with increased positive end-expiratory pressure may help to "tamponade" or slow the bleeding and permit oxygenation. The diagnostic approach and management of severe hemoptysis in children is discussed in detail separately. (See "Hemoptysis in children", section on 'Initial assessment and control of bleeding' and "Hemoptysis in children", section on 'Control of life-threatening hemoptysis'.)

Vascular access — Adequate vascular access must be obtained for rapid infusion of fluid. Two peripheral intravenous catheters consisting of the largest bore, shortest length, that can be reliably placed (22 to 24 gauge in newborns and infants, 18 to 20 gauge for older children) typically suffice. Ideally, at least one of the two access sites should be above the diaphragm (upper extremity, external jugular vein, or scalp vein) in the event that the patient has diminished inferior vena cava blood return due to traumatic disruption or extrinsic compression. (See "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies", section on 'Catheter selection'.)

For children in shock, intraosseous cannulation should be performed if intravenous access cannot be established quickly. During cardiopulmonary resuscitation (CPR) or the treatment of severe shock, intraosseous cannulation, and peripheral venous access should be pursued simultaneously [3]. (See "Intraosseous infusion", section on 'Indications'.)

Fluid resuscitation — The goal of fluid therapy is rapid restoration of intravascular volume. Children with hypovolemic shock should receive isotonic crystalloid, such as normal saline or Lactated Ringer solution. (See "Initial management of shock in children".)

Limited evidence exists concerning the optimal amount and rate of fluid administration for children with hypovolemic shock although aggressive fluid resuscitation is associated with improved outcomes in children with hypotensive septic shock. (See "Initial management of shock in children", section on 'Volume and rate'.)

The degree of hypovolemic shock determines the volume and rate of initial fluid administration (see "Initial management of shock in children", section on 'Volume and rate'):

Children with hypotensive hypovolemic shock should receive 20 mL/kg per bolus of isotonic crystalloid, such as normal saline or Lactated Ringer solution, infused over 5 to 10 minutes and repeated, as needed, up to three times in patients without improvement and no signs of fluid overload. Additional therapies, such as blood transfusion in patients with hypovolemic shock from hemorrhage, may be required depending upon the response to fluid administration.

Techniques to rapidly deliver intravenous fluid include applying pressure directly to the bag of fluid with an inflatable device, delivering aliquots of fluid using a large syringe that is refilled through a three-way stopcock attached to the bag (the "push-pull" method), or use of rapid infusion pumps designed to deliver high volumes of warmed fluids or blood. Gravity alone is unlikely to deliver 20 mL/kg over 5 to 10 minutes. Standard infusion pumps are also unable to provide a sufficiently rapid rate of fluid delivery.

Children with compensated hypovolemic shock may receive 20 mL/kg per bolus of isotonic crystalloid, such as normal saline or Lactated Ringer solution, over 5 to 20 minutes. Patients should be closely monitored during fluid administration. Additional fluid boluses may be indicated depending upon the patient's response.

After the initial fluid bolus, the following physiologic indicators of perfusion (with therapeutic goals in parentheses) should be evaluated:

Mental status (normal mental status)

Quality of central and peripheral pulses (strong, distal pulses equal to central pulses)

Skin perfusion (warm, with capillary refill <2 seconds)

Urine output (≥1 mL/kg per hour, once effective circulating volume is restored)

Blood pressure (systolic pressure at least fifth percentile for age: 60 mmHg <1 month of age, 70 mmHg + [2 x age in years] in children 1 month to 10 years of age, 90 mmHg in children 10 years of age or older)

Abnormalities in blood glucose, electrolyte, and calcium measurements should be identified and treatment initiated. Children who have not improved should continue to receive isotonic crystalloid in 20 mL/kg boluses to a total of 60 mL/kg, ideally within the first 30 to 60 minutes of treatment. Patients with hemorrhagic shock typically require 3 mL of crystalloid to replace each milliliter of blood lost [12].

Patients should be examined for physiologic indicators of peripheral perfusion and signs of fluid overload (decreased oxygenation, crackles, gallop rhythm, hepatomegaly) before and after each bolus.

In most children with hypovolemic shock, rapid improvement occurs with initial fluid administration. Children who have not improved after receiving a total of 60 mL/kg of isotonic fluid should be evaluated for other causes of shock. Patients with apparent nonhemorrhagic hypovolemic shock may have associated conditions (eg, septic shock, heart failure from myocarditis). Children with traumatic hemorrhagic shock may have additional injuries (ie, spinal cord injury). (See "Initial evaluation of shock in children" and "Initial management of shock in children".)

Further management considerations for children who have not improved after receiving 60 mL/kg of isotonic fluid include:

Patients with hemorrhagic shock should receive blood and require definitive treatment for the cause of hemorrhage. Packed red blood cells should be infused in 10 mL/kg boluses. Delayed fluid resuscitation for traumatic hemorrhagic is not recommended for children. (See "Trauma management: Approach to the unstable child", section on 'Controlled hypotension'.)

For children with nonhemorrhagic hypovolemic shock, the amount of fluid loss may have been underestimated (as with burn injury) or there may be significant ongoing fluid loss (ie, from capillary leak with bowel obstruction). (See "Moderate and severe thermal burns in children: Emergency management", section on 'Evaluation of burn injury'.)

Colloid administration may be an option for patients with decreased arterial volume related to low intravascular oncotic pressure (as in nephrotic syndrome or other causes of hypoalbuminemia). However, randomized trials and meta-analyses have failed to consistently demonstrate a difference in clinical outcomes for adults and children receiving colloid therapy for shock when compared to continue crystalloid infusion. (See "Treatment of hypovolemia (dehydration) in children in resource-abundant settings", section on 'Crystalloid versus colloid' and "Treatment of severe hypovolemia or hypovolemic shock in adults", section on 'Normal saline (crystalloid)'.)

Vasoactive medications have no place in the treatment of isolated hypovolemic shock. These interventions do not address the underlying problem of inadequate circulating blood volume and may worsen tissue hypoxia [3,12].

On the other hand, patients with septic shock who do require vasoactive medications often have concomitant hypovolemia and warrant aggressive fluid resuscitation. (See "Septic shock in children: Rapid recognition and initial resuscitation (first hour)", section on 'Fluid resuscitation'.)

Glucose abnormalities — Hypoglycemia should be corrected by rapid intravenous infusion of dextrose as described in the rapid overview (table 5). Patients who should not have oral intake (eg, hemorrhagic shock from trauma) should have hypoglycemia corrected by intravenous dextrose infusion.

For patients with stress hyperglycemia, treatment of the underlying condition typically suffices. As an example, among 72 critically ill patients, including trauma victims, with extreme stress hyperglycemia (blood glucose >300 mg/dL [16.7 mmol/L]), glucose concentrations decreased to ≤150 mg/dL (8.3 mmol/L) in 67 percent within 48 hours [4]. Only eight of these patients received insulin or intravenous fluids without glucose to treat hyperglycemia.

Ongoing management — Once intravascular volume is restored and the patient's condition is stabilized, ongoing management is determined by the underlying condition. For children with hemorrhagic shock, the source of bleeding must be identified and controlled [12,13].

For those with nonhemorrhagic shock, the cause must be identified and treated (ie, relieving bowel obstruction with intussusception). Ongoing fluid therapy consists of repletion of deficit and ongoing losses and administration of maintenance requirements (table 6). The sodium content of repletion fluid and the rate of correction are dependent upon the serum sodium (see "Treatment of hypovolemia (dehydration) in children in resource-abundant settings", section on 'Therapy according to serum sodium' and "Maintenance intravenous fluid therapy in children"):

For patients who are normonatremic, the fluid deficit should be replaced with isotonic saline. The serum sodium concentration should not change substantially with repletion therapy, as sodium and water are given in proportion.

Children with mild to moderate hyponatremia can be treated with isotonic saline alone, similar to normonatremic patients.

With severe hyponatremia, correction of serum sodium at a rate of about 0.5 mEq/L per hour is recommended to avoid the development of osmotic demyelination and irreversible neurologic injury. For patients with neurologic symptoms (ie, obtundation or active seizures), however, an initial goal of raising the serum sodium by 5 mEq/L over the first three to four hours by administering hypertonic saline (eg, 3 percent saline) is preferred because the risk of delayed therapy is greater than the risk of osmotic demyelination from overly rapid correction. (See "Treatment of hypovolemia (dehydration) in children in resource-abundant settings", section on 'Therapy according to serum sodium' and "Overview of the treatment of hyponatremia in adults".)

The goals of therapy in children with hypovolemia and a serum sodium above 155 mEq/L are correction of the volume deficit and gradual correction of the hypernatremia at a rate of less than 12 mEq/L per day (less than 0.5 mEq/L per hour). Rapid correction of hypernatremia causes osmotic water movement into the brain, resulting in cerebral edema, which can lead to seizures, permanent neurologic damage, or death. (See "Treatment of hypovolemia (dehydration) in children in resource-abundant settings", section on 'Therapy according to serum sodium'.)

Fluid resuscitation in children with moderate to severe burns is discussed separately. (See "Moderate and severe thermal burns in children: Emergency management", section on 'Fluid resuscitation'.)

Disposition — Children with hypovolemic shock warrant inpatient admission and ongoing evaluation, monitoring, and treatment. Those who have traumatic hemorrhagic shock require management by a surgical team with expertise in pediatric trauma. (See "Trauma management: Approach to the unstable child", section on 'Definitive care'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Shock in children".)

SUMMARY AND RECOMMENDATIONS

Hypovolemic shock is characterized by inadequate tissue perfusion from decreased intravascular volume as the result of fluid loss and/or inadequate fluid intake. Sources of volume loss include intravascular volume (as with hemorrhage, capillary leak, and third space losses from intraabdominal pathology [eg, pancreatitis, intussusception, small bowel obstruction]), extravascular fluid (as with vomiting, diarrhea, and osmotic diuresis), and insensible losses (moderate to severe burns). (See 'Etiology' above and 'Pathophysiology and classification' above.)

Among children in shock, compensatory mechanisms (ie, tachycardia, increased systemic vascular resistance, and increased cardiac contractility) typically maintain blood pressure until intravascular volume is decreased by 30 percent or more. Hypotension develops late and progresses rapidly to cardiovascular collapse. Clinical features can be used to estimate the amount of fluid lost (table 1 and table 2). (See 'Pathophysiology and classification' above.)

An approach to rapidly identifying the cause of shock based upon clinical findings is provided in the algorithm (algorithm 1). Evaluation includes identification and stabilization of life-threatening conditions and identifying the source and amount of volume loss. (See 'Evaluation' above.)

Laboratory evaluation may identify metabolic abnormalities (ie, hypoglycemia or hypernatremia) that require treatment. Hypoperfusion should be suspected when the lactate is >2 mmol/L (18 mg/dL). Initial lactate levels >4.0 mmol/L (36 mg/dL) are associated with increased mortality in children. Hypoglycemia should be corrected by rapid intravenous infusion of dextrose as described in the rapid overview (table 5). Children with hemorrhagic shock may require transfusion and should have samples sent to the blood bank for type and cross match. (See 'Laboratory evaluation' above.)

Successful management of children with hypovolemic shock requires identification and treatment of life-threatening conditions and the rapid initiation of aggressive fluid resuscitation:

Cervical spine immobilization should be performed for children with traumatic hemorrhagic shock until a spinal fracture is ruled out. (See 'Airway and breathing' above.)

Airway management should include supplemental oxygen with an initial inspired concentration of 100 percent. Early positive pressure ventilation and intubation should be performed in patients with airway compromise or impending respiratory failure. A rapid overview provides the suggested approach to rapid sequence intubation in children (table 4). (See 'Airway and breathing' above.)

Sites of significant external hemorrhage require direct manual pressure to control bleeding (figure 1). In patients whose bleeding does not abate with direct pressure or who have a sharp foreign body at the site of bleeding or an amputation, compression at the nearest vascular pressure point provides an alternative means for hemorrhage control (figure 2). (See 'Control of hemorrhage' above.)

Adequate vascular access must be obtained for rapid infusion of fluid. Two peripheral intravenous catheters consisting of the largest size that can be reliably placed (22 to 24 gauge in newborns and infants, 18 to 20 gauge for older children) typically suffice. For children in shock, intraosseous cannulation should be performed if intravenous access cannot be established quickly. (See 'Vascular access' above.)

Fluid resuscitation includes the administration of isotonic crystalloid in 20 mL/kg boluses, followed by evaluation of physiologic indicators of peripheral perfusion (blood pressure, quality of central and peripheral pulses, skin perfusion, mental status, and urine output). (See 'Fluid resuscitation' above.)

Hypoglycemia should be corrected by rapid intravenous infusion of dextrose as described in the rapid overview (table 5). For patients with stress hyperglycemia, treatment of the underlying condition typically suffices. (See 'Glucose abnormalities' above.)

Children who have not improved after receiving a total of 60 mL/kg of isotonic fluid should be evaluated for ongoing blood loss or other causes of shock. (See 'Fluid resuscitation' above.)

For children with nonhemorrhagic shock, the sodium content of repletion fluid and the rate of correction are dependent upon the serum sodium. (See 'Ongoing management' above.)

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  3. Pediatric Advanced Life Support Provider Manual, American Heart Association, Dallas 2020.
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  5. Hatherill M, Waggie Z, Purves L, et al. Mortality and the nature of metabolic acidosis in children with shock. Intensive Care Med 2003; 29:286.
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  7. Patregnani JT, Borgman MA, Maegele M, et al. Coagulopathy and shock on admission is associated with mortality for children with traumatic injuries at combat support hospitals. Pediatr Crit Care Med 2012; 13:273.
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  9. O'Brien AJ, Brady RM. Point-of-care ultrasound in paediatric emergency medicine. J Paediatr Child Health 2016; 52:174.
  10. Leonard J, Zietlow J, Morris D, et al. A multi-institutional study of hemostatic gauze and tourniquets in rural civilian trauma. J Trauma Acute Care Surg 2016; 81:441.
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Topic 6389 Version 23.0

References

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